Genome-wide mapping of immature erythrocyte transcribed chromosomal domains (F1-seq)
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ABSTRACT:
ORGANISM(S): Gallus gallus
SUBMITTER: wayne xu
PROVIDER: E-GEOD-75849 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional regulation is impacted by multiple layers of genome organization. Here, we identified and mapped out all the transcriptionally active chromosomal domains in the chicken immature erythrocyte genome, including the known β- and α-globin domains, by combining a powerful chromatin fractionation method with next generation DNA and RNA sequencing. Two biological replicates of total RNA were sequenced to characterize genes in chicken erythrocyte cells
2016-07-03 | E-GEOD-75848 | biostudies-arrayexpress
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2010-05-19 | E-GEOD-18898 | biostudies-arrayexpress
Project description:Expression of CD40 in non-hematopoietic cells has been linked to inflammation. We presented evidence that CD40, a T-cell costimulatory molecule, is expressed in human β-cells and the engagement of CD40 in insulinoma cells activated the NFKB and ERK1/2 pathways. CD40 activation in human islets cells induced secretion of IL-8, MCP-1 and MIP-1 β, which is abrogated by inhibitors of NFkB and ERK1/2 inhibitors. In this study, we have studied gene expression mediated by CD40-CD40L interaction in islet cells. This approach identified 90 genes and transcripts exhibiting at least a 1.7 fold increase in their expression intensity after treatment with soluble CD40L. A significant number of genes were related to inflammation and oxidative stress. We have a strong overexpression of CXCL1 (Groα), CXCL2 (Mif2) and CXCL3; chemokines belonging to CXC family structurally related to Il-8. 11 genes were selected from this group and further quantified by Real Time PCR, including CXCL1. Activation of islet cells with CD40L induced the secretion of CXCL1 in a NFKB dependent manner. Engagement of CD40 in islet cells did not induce apoptosis, neither β-cell death and did not enhanced TNF-α mediated cell death as observed in insulinoma cells. CD40 activation in insulinoma cells, results in ERK1/2 dependent phsophorylation of synapsin I, a protein associated with the exocytosis machinery in neurons and β-cells. However, treatment of islets with soluble CD40L did not affect glucose induced insulin secretion. It has been reported that ductal cells always present in human islet preparations express CD40 constitutively (ref). We found that CD40-CD40L interaction in ductal cells, unlike in β-cells, induces secretion of diabetogenic cytokines IFNγ and TNF-α. Furthermore, incubation of islets containing ductal cells with CD40L decreased β-cells viability as assessed by measurement of their mitochondrial membrane potential Experiment Overall Design: We isolated islet cells from three patients. Part of islet cells from each patient has been treated with CD40L. We compared gene expression in treated cells vs untreated for each patient using dye-swap.
2008-10-20 | E-GEOD-8873 | biostudies-arrayexpress
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Project description:Embedded in the nuclear envelope, nuclear pore complexes (NPCs) not only regulate nuclear transport, but also interface with both transcriptionally active euchromatin and largely silenced heterochromatin, as well as the boundaries between these regions. It is unclear what functional role NPCs play in establishing or maintaining these distinct chromatin domains. Here we report that the yeast NPC protein Nup170p interacts with specific regions of the genome containing ribosomal protein and subtelomeric genes. At these locations, Nup170p functions to establish normal nucleosome positioning and as a repressor of transcription. We show that the function of Nup170p in subtelomeric gene silencing is linked to its association with the RSC chromatin-remodeling complex and the silencing factor Sir4p, and that the binding of Nup170p and Sir4p to subtelomeric chromatin is cooperative and necessary for the association of telomeres with the nuclear envelope. Our results establish the NPC as an active participant in the formation of peripheral heterochromatin. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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Project description:A conspicuous feature of early animal development is the lack of transcription from the embryonic genome, and it typically takes several hours to several days (depending on the species) until widespread transcription of the embryonic genome begins. Although this transition is ubiquitous, relatively little is known about how the shift from a transcriptionally quiescent to transcriptionally active genome is controlled. We describe here the genome-wide distributions and temporal dynamics of nucleosomes and post-translational histone modifications through the maternal-to-zygotic transition in embryos of the pomace fly Drosophila melanogaster. At mitotic cycle 8, when few zygotic genes are being transcribed, embryonic chromatin is in a relatively simple state: there are few nucleosome-free regions, undetectable levels of the histone methylation marks characteristic of mature chromatin, and low levels of histone acetylation at a relatively small number of loci. Histone acetylation increases by cycle 12, but it is not until cycle 14 that nucleosome-free regions and domains of histone methylation become widespread. Early histone acetylation is strongly associated with regions that we have previously shown are bound in early embryos by the maternally deposited transcription factor Zelda. Most of these Zelda-bound regions are destined to be enhancers or promoters active during mitotic cycle 14, and our data demonstrate that they are biochemically distinct long before they become active, raising the possibility that Zelda triggers a cascade of events, including the accumulation of specific histone modifications, that plays a role in the subsequent activation of these sequences. Many of these Zelda-associated active regions occur in larger domains that we find strongly enriched for histone marks characteristic of Polycomb-mediated repression, suggesting a dynamic balance between Zelda activation and Polycomb repression. Collectively, these data paint a complex picture of a genome in transition from a quiescent to an active state, and highlight the role of Zelda in mediating this transition. We performed genome-wide mapping of histone H3 and 9 types of histone modifications, including H4K5ac, H4K8ac, H3K4me1, H3K4me3, H3K27me3, H3K36me3, H3K9ac, H3K18ac, and H3K27ac by ChIP-seq, in hand-sorted wild-type Drosophila melanogaster embryos at 4 different development time points corresponding to mitotic cycle 7-9, 11-13, 14a-b, and 14c-d, respectively. We also carried out ChIP-seq experiments in zelda mutant embryos after showing that the deposition of histone marks in early embryos strongly correlated with the binding of Zelda in wild-type embryos.
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